Journal of the renin-angiotensin-aldosterone system : JRAAS · 2020
Association of angiotensin-converting enzyme gene insertion/deletion polymorphism and obstructive sleep apnoea in a Chinese population: A meta-analysis.
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Xu Jian, Chen Jiming, Li Yilu, Zhang Dandan, Li Xiaoli
Аннотация
INTRODUCTION: Many studies have investigated the association between angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and susceptibility to obstructive sleep apnoea (OSA). However, few have confirmed the relationship between ACE and OSA in the Chinese population. We performed a meta-analysis of studies relating the ACE I/D polymorphism to the risk of OSA in a Chinese population.
METHODS: We evaluated eligible published studies from several databases for this meta-analysis. Subgroup analyses were performed for hypertension. Pooled odds ratios and 95% confidence intervals were calculated using a fixed- or random-effects model.
RESULTS: Ten studies were identified to analyse the association between ACE I/D polymorphism and OSA risk. No marked associations were found in any genetic model (p>0.05). Subgroup analysis showed an association with hypertension (D vs. I, DD vs. II, ID vs. DD+II, DD+ID vs. II, ID vs. II; p<0.05), which was confirmed by sensitivity analyses. No obvious publication bias was found using Egger's test (p>0.05).
CONCLUSIONS: The ACE I/D polymorphism was not associated with an increased risk of OSA in a Chinese population. However, within the hypertensive subgroup, we detected a significant association between the ACE polymorphism and OSA. More case-control investigations are required.
METHODS: We evaluated eligible published studies from several databases for this meta-analysis. Subgroup analyses were performed for hypertension. Pooled odds ratios and 95% confidence intervals were calculated using a fixed- or random-effects model.
RESULTS: Ten studies were identified to analyse the association between ACE I/D polymorphism and OSA risk. No marked associations were found in any genetic model (p>0.05). Subgroup analysis showed an association with hypertension (D vs. I, DD vs. II, ID vs. DD+II, DD+ID vs. II, ID vs. II; p<0.05), which was confirmed by sensitivity analyses. No obvious publication bias was found using Egger's test (p>0.05).
CONCLUSIONS: The ACE I/D polymorphism was not associated with an increased risk of OSA in a Chinese population. However, within the hypertensive subgroup, we detected a significant association between the ACE polymorphism and OSA. More case-control investigations are required.